PMC:7195088 / 48338-49579 JSONTXT

{"project":"LitCovid-PubTator","denotations":[{"id":"1458","span":{"begin":588,"end":615},"obj":"Gene"},{"id":"1459","span":{"begin":617,"end":635},"obj":"Gene"},{"id":"1460","span":{"begin":57,"end":65},"obj":"Species"},{"id":"1461","span":{"begin":297,"end":305},"obj":"Species"},{"id":"1462","span":{"begin":312,"end":322},"obj":"Species"},{"id":"1463","span":{"begin":428,"end":431},"obj":"Species"},{"id":"1464","span":{"begin":845,"end":853},"obj":"Species"},{"id":"1465","span":{"begin":1225,"end":1235},"obj":"Species"},{"id":"1466","span":{"begin":23,"end":34},"obj":"Chemical"},{"id":"1467","span":{"begin":215,"end":226},"obj":"Chemical"},{"id":"1468","span":{"begin":687,"end":698},"obj":"Chemical"},{"id":"1469","span":{"begin":1035,"end":1053},"obj":"Chemical"},{"id":"1470","span":{"begin":1079,"end":1090},"obj":"Chemical"},{"id":"1471","span":{"begin":48,"end":56},"obj":"Disease"},{"id":"1472","span":{"begin":825,"end":844},"obj":"Disease"},{"id":"1473","span":{"begin":1141,"end":1149},"obj":"Disease"}],"attributes":[{"id":"A1458","pred":"tao:has_database_id","subj":"1458","obj":"Gene:7124"},{"id":"A1459","pred":"tao:has_database_id","subj":"1459","obj":"Gene:3569"},{"id":"A1460","pred":"tao:has_database_id","subj":"1460","obj":"Tax:9606"},{"id":"A1461","pred":"tao:has_database_id","subj":"1461","obj":"Tax:694009"},{"id":"A1462","pred":"tao:has_database_id","subj":"1462","obj":"Tax:2697049"},{"id":"A1463","pred":"tao:has_database_id","subj":"1463","obj":"Tax:11118"},{"id":"A1464","pred":"tao:has_database_id","subj":"1464","obj":"Tax:9606"},{"id":"A1465","pred":"tao:has_database_id","subj":"1465","obj":"Tax:2697049"},{"id":"A1466","pred":"tao:has_database_id","subj":"1466","obj":"MESH:D002738"},{"id":"A1467","pred":"tao:has_database_id","subj":"1467","obj":"MESH:D002738"},{"id":"A1468","pred":"tao:has_database_id","subj":"1468","obj":"MESH:D002738"},{"id":"A1469","pred":"tao:has_database_id","subj":"1469","obj":"MESH:D006886"},{"id":"A1470","pred":"tao:has_database_id","subj":"1470","obj":"MESH:D002738"},{"id":"A1471","pred":"tao:has_database_id","subj":"1471","obj":"MESH:C000657245"},{"id":"A1472","pred":"tao:has_database_id","subj":"1472","obj":"MESH:C000657245"},{"id":"A1473","pred":"tao:has_database_id","subj":"1473","obj":"MESH:D064420"}],"namespaces":[{"prefix":"Tax","uri":"https://www.ncbi.nlm.nih.gov/taxonomy/"},{"prefix":"MESH","uri":"https://id.nlm.nih.gov/mesh/"},{"prefix":"Gene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"CVCL","uri":"https://web.expasy.org/cellosaurus/CVCL_"}],"text":"The rationale of using chloroquine for treating COVID-19 patients is based on two potential and non–mutually exclusive mechanisms: antiviral activity and immunomodulatory effects. With regard to antiviral activity, chloroquine has been shown to inhibit various viruses in cell cultures, including SARS-CoV-1 and SARS-CoV-2, possibly via pH-dependent inhibition of virus–endosome fusion and/or posttranslational modifications of CoV proteins, although other mechanisms may also contribute [[32], [33], [34], [35]]. With regard to the immunomodulatory effects, the attenuated production of tumor necrosis factor alpha, interleukin (IL)-6 and interferons that follows the administration of chloroquine might help counteract an exaggerated proinflammatory response, which is thought to contribute to the organ damage observed in SARS-CoV-2–infected patients [36,37]. However, some authors have pointed out that an unfavourable immunomodulatory effect cannot be excluded, based on a reduced T helper 2 differentiation [38]. In our opinion, hydroxychloroquine should be preferred over chloroquine because of its less toxic profile (reduced ocular toxicity and fewer drug interactions) and its more potent in vitro activity against SARS-CoV-2 [39]."}

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T85","span":{"begin":272,"end":276},"obj":"Body_part"},{"id":"T86","span":{"begin":370,"end":378},"obj":"Body_part"},{"id":"T87","span":{"begin":432,"end":440},"obj":"Body_part"},{"id":"T88","span":{"begin":617,"end":628},"obj":"Body_part"},{"id":"T89","span":{"begin":630,"end":632},"obj":"Body_part"},{"id":"T90","span":{"begin":800,"end":805},"obj":"Body_part"}],"attributes":[{"id":"A85","pred":"fma_id","subj":"T85","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A86","pred":"fma_id","subj":"T86","obj":"http://purl.org/sig/ont/fma/fma67180"},{"id":"A87","pred":"fma_id","subj":"T87","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A88","pred":"fma_id","subj":"T88","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A89","pred":"fma_id","subj":"T89","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A90","pred":"fma_id","subj":"T90","obj":"http://purl.org/sig/ont/fma/fma67498"}],"text":"The rationale of using chloroquine for treating COVID-19 patients is based on two potential and non–mutually exclusive mechanisms: antiviral activity and immunomodulatory effects. With regard to antiviral activity, chloroquine has been shown to inhibit various viruses in cell cultures, including SARS-CoV-1 and SARS-CoV-2, possibly via pH-dependent inhibition of virus–endosome fusion and/or posttranslational modifications of CoV proteins, although other mechanisms may also contribute [[32], [33], [34], [35]]. With regard to the immunomodulatory effects, the attenuated production of tumor necrosis factor alpha, interleukin (IL)-6 and interferons that follows the administration of chloroquine might help counteract an exaggerated proinflammatory response, which is thought to contribute to the organ damage observed in SARS-CoV-2–infected patients [36,37]. However, some authors have pointed out that an unfavourable immunomodulatory effect cannot be excluded, based on a reduced T helper 2 differentiation [38]. In our opinion, hydroxychloroquine should be preferred over chloroquine because of its less toxic profile (reduced ocular toxicity and fewer drug interactions) and its more potent in vitro activity against SARS-CoV-2 [39]."}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T45","span":{"begin":800,"end":805},"obj":"Body_part"}],"attributes":[{"id":"A45","pred":"uberon_id","subj":"T45","obj":"http://purl.obolibrary.org/obo/UBERON_0000062"}],"text":"The rationale of using chloroquine for treating COVID-19 patients is based on two potential and non–mutually exclusive mechanisms: antiviral activity and immunomodulatory effects. With regard to antiviral activity, chloroquine has been shown to inhibit various viruses in cell cultures, including SARS-CoV-1 and SARS-CoV-2, possibly via pH-dependent inhibition of virus–endosome fusion and/or posttranslational modifications of CoV proteins, although other mechanisms may also contribute [[32], [33], [34], [35]]. With regard to the immunomodulatory effects, the attenuated production of tumor necrosis factor alpha, interleukin (IL)-6 and interferons that follows the administration of chloroquine might help counteract an exaggerated proinflammatory response, which is thought to contribute to the organ damage observed in SARS-CoV-2–infected patients [36,37]. However, some authors have pointed out that an unfavourable immunomodulatory effect cannot be excluded, based on a reduced T helper 2 differentiation [38]. In our opinion, hydroxychloroquine should be preferred over chloroquine because of its less toxic profile (reduced ocular toxicity and fewer drug interactions) and its more potent in vitro activity against SARS-CoV-2 [39]."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T86","span":{"begin":588,"end":593},"obj":"Phenotype"}],"attributes":[{"id":"A86","pred":"hp_id","subj":"T86","obj":"http://purl.obolibrary.org/obo/HP_0002664"}],"text":"The rationale of using chloroquine for treating COVID-19 patients is based on two potential and non–mutually exclusive mechanisms: antiviral activity and immunomodulatory effects. With regard to antiviral activity, chloroquine has been shown to inhibit various viruses in cell cultures, including SARS-CoV-1 and SARS-CoV-2, possibly via pH-dependent inhibition of virus–endosome fusion and/or posttranslational modifications of CoV proteins, although other mechanisms may also contribute [[32], [33], [34], [35]]. With regard to the immunomodulatory effects, the attenuated production of tumor necrosis factor alpha, interleukin (IL)-6 and interferons that follows the administration of chloroquine might help counteract an exaggerated proinflammatory response, which is thought to contribute to the organ damage observed in SARS-CoV-2–infected patients [36,37]. However, some authors have pointed out that an unfavourable immunomodulatory effect cannot be excluded, based on a reduced T helper 2 differentiation [38]. In our opinion, hydroxychloroquine should be preferred over chloroquine because of its less toxic profile (reduced ocular toxicity and fewer drug interactions) and its more potent in vitro activity against SARS-CoV-2 [39]."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T268","span":{"begin":48,"end":56},"obj":"Disease"},{"id":"T269","span":{"begin":297,"end":305},"obj":"Disease"},{"id":"T270","span":{"begin":312,"end":320},"obj":"Disease"},{"id":"T271","span":{"begin":588,"end":593},"obj":"Disease"},{"id":"T272","span":{"begin":825,"end":833},"obj":"Disease"},{"id":"T273","span":{"begin":1225,"end":1233},"obj":"Disease"}],"attributes":[{"id":"A268","pred":"mondo_id","subj":"T268","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A269","pred":"mondo_id","subj":"T269","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A270","pred":"mondo_id","subj":"T270","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A271","pred":"mondo_id","subj":"T271","obj":"http://purl.obolibrary.org/obo/MONDO_0005070"},{"id":"A272","pred":"mondo_id","subj":"T272","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A273","pred":"mondo_id","subj":"T273","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"}],"text":"The rationale of using chloroquine for treating COVID-19 patients is based on two potential and non–mutually exclusive mechanisms: antiviral activity and immunomodulatory effects. With regard to antiviral activity, chloroquine has been shown to inhibit various viruses in cell cultures, including SARS-CoV-1 and SARS-CoV-2, possibly via pH-dependent inhibition of virus–endosome fusion and/or posttranslational modifications of CoV proteins, although other mechanisms may also contribute [[32], [33], [34], [35]]. With regard to the immunomodulatory effects, the attenuated production of tumor necrosis factor alpha, interleukin (IL)-6 and interferons that follows the administration of chloroquine might help counteract an exaggerated proinflammatory response, which is thought to contribute to the organ damage observed in SARS-CoV-2–infected patients [36,37]. However, some authors have pointed out that an unfavourable immunomodulatory effect cannot be excluded, based on a reduced T helper 2 differentiation [38]. In our opinion, hydroxychloroquine should be preferred over chloroquine because of its less toxic profile (reduced ocular toxicity and fewer drug interactions) and its more potent in vitro activity against SARS-CoV-2 [39]."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T277","span":{"begin":141,"end":149},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T278","span":{"begin":205,"end":213},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T279","span":{"begin":227,"end":230},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T280","span":{"begin":261,"end":268},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T281","span":{"begin":272,"end":276},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T282","span":{"begin":364,"end":369},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T283","span":{"begin":502,"end":504},"obj":"http://purl.obolibrary.org/obo/CLO_0001302"},{"id":"T284","span":{"begin":508,"end":510},"obj":"http://purl.obolibrary.org/obo/CLO_0001000"},{"id":"T285","span":{"begin":588,"end":615},"obj":"http://purl.obolibrary.org/obo/PR_000000134"},{"id":"T286","span":{"begin":800,"end":805},"obj":"http://purl.obolibrary.org/obo/UBERON_0003103"},{"id":"T287","span":{"begin":976,"end":977},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T288","span":{"begin":1208,"end":1216},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"}],"text":"The rationale of using chloroquine for treating COVID-19 patients is based on two potential and non–mutually exclusive mechanisms: antiviral activity and immunomodulatory effects. With regard to antiviral activity, chloroquine has been shown to inhibit various viruses in cell cultures, including SARS-CoV-1 and SARS-CoV-2, possibly via pH-dependent inhibition of virus–endosome fusion and/or posttranslational modifications of CoV proteins, although other mechanisms may also contribute [[32], [33], [34], [35]]. With regard to the immunomodulatory effects, the attenuated production of tumor necrosis factor alpha, interleukin (IL)-6 and interferons that follows the administration of chloroquine might help counteract an exaggerated proinflammatory response, which is thought to contribute to the organ damage observed in SARS-CoV-2–infected patients [36,37]. However, some authors have pointed out that an unfavourable immunomodulatory effect cannot be excluded, based on a reduced T helper 2 differentiation [38]. In our opinion, hydroxychloroquine should be preferred over chloroquine because of its less toxic profile (reduced ocular toxicity and fewer drug interactions) and its more potent in vitro activity against SARS-CoV-2 [39]."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T584","span":{"begin":23,"end":34},"obj":"Chemical"},{"id":"T585","span":{"begin":131,"end":140},"obj":"Chemical"},{"id":"T586","span":{"begin":195,"end":204},"obj":"Chemical"},{"id":"T587","span":{"begin":215,"end":226},"obj":"Chemical"},{"id":"T588","span":{"begin":432,"end":440},"obj":"Chemical"},{"id":"T589","span":{"begin":610,"end":615},"obj":"Chemical"},{"id":"T590","span":{"begin":630,"end":632},"obj":"Chemical"},{"id":"T592","span":{"begin":687,"end":698},"obj":"Chemical"},{"id":"T593","span":{"begin":1035,"end":1053},"obj":"Chemical"},{"id":"T594","span":{"begin":1079,"end":1090},"obj":"Chemical"},{"id":"T595","span":{"begin":1160,"end":1164},"obj":"Chemical"}],"attributes":[{"id":"A584","pred":"chebi_id","subj":"T584","obj":"http://purl.obolibrary.org/obo/CHEBI_3638"},{"id":"A585","pred":"chebi_id","subj":"T585","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"},{"id":"A586","pred":"chebi_id","subj":"T586","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"},{"id":"A587","pred":"chebi_id","subj":"T587","obj":"http://purl.obolibrary.org/obo/CHEBI_3638"},{"id":"A588","pred":"chebi_id","subj":"T588","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A589","pred":"chebi_id","subj":"T589","obj":"http://purl.obolibrary.org/obo/CHEBI_30216"},{"id":"A590","pred":"chebi_id","subj":"T590","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A591","pred":"chebi_id","subj":"T590","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A592","pred":"chebi_id","subj":"T592","obj":"http://purl.obolibrary.org/obo/CHEBI_3638"},{"id":"A593","pred":"chebi_id","subj":"T593","obj":"http://purl.obolibrary.org/obo/CHEBI_5801"},{"id":"A594","pred":"chebi_id","subj":"T594","obj":"http://purl.obolibrary.org/obo/CHEBI_3638"},{"id":"A595","pred":"chebi_id","subj":"T595","obj":"http://purl.obolibrary.org/obo/CHEBI_23888"}],"text":"The rationale of using chloroquine for treating COVID-19 patients is based on two potential and non–mutually exclusive mechanisms: antiviral activity and immunomodulatory effects. With regard to antiviral activity, chloroquine has been shown to inhibit various viruses in cell cultures, including SARS-CoV-1 and SARS-CoV-2, possibly via pH-dependent inhibition of virus–endosome fusion and/or posttranslational modifications of CoV proteins, although other mechanisms may also contribute [[32], [33], [34], [35]]. With regard to the immunomodulatory effects, the attenuated production of tumor necrosis factor alpha, interleukin (IL)-6 and interferons that follows the administration of chloroquine might help counteract an exaggerated proinflammatory response, which is thought to contribute to the organ damage observed in SARS-CoV-2–infected patients [36,37]. However, some authors have pointed out that an unfavourable immunomodulatory effect cannot be excluded, based on a reduced T helper 2 differentiation [38]. In our opinion, hydroxychloroquine should be preferred over chloroquine because of its less toxic profile (reduced ocular toxicity and fewer drug interactions) and its more potent in vitro activity against SARS-CoV-2 [39]."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T15","span":{"begin":393,"end":424},"obj":"http://purl.obolibrary.org/obo/GO_0043687"},{"id":"T16","span":{"begin":594,"end":602},"obj":"http://purl.obolibrary.org/obo/GO_0070265"},{"id":"T17","span":{"begin":594,"end":602},"obj":"http://purl.obolibrary.org/obo/GO_0019835"},{"id":"T18","span":{"begin":594,"end":602},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T19","span":{"begin":594,"end":602},"obj":"http://purl.obolibrary.org/obo/GO_0001906"}],"text":"The rationale of using chloroquine for treating COVID-19 patients is based on two potential and non–mutually exclusive mechanisms: antiviral activity and immunomodulatory effects. With regard to antiviral activity, chloroquine has been shown to inhibit various viruses in cell cultures, including SARS-CoV-1 and SARS-CoV-2, possibly via pH-dependent inhibition of virus–endosome fusion and/or posttranslational modifications of CoV proteins, although other mechanisms may also contribute [[32], [33], [34], [35]]. With regard to the immunomodulatory effects, the attenuated production of tumor necrosis factor alpha, interleukin (IL)-6 and interferons that follows the administration of chloroquine might help counteract an exaggerated proinflammatory response, which is thought to contribute to the organ damage observed in SARS-CoV-2–infected patients [36,37]. However, some authors have pointed out that an unfavourable immunomodulatory effect cannot be excluded, based on a reduced T helper 2 differentiation [38]. In our opinion, hydroxychloroquine should be preferred over chloroquine because of its less toxic profile (reduced ocular toxicity and fewer drug interactions) and its more potent in vitro activity against SARS-CoV-2 [39]."}

{"project":"LitCovid-sentences","denotations":[{"id":"T376","span":{"begin":0,"end":179},"obj":"Sentence"},{"id":"T377","span":{"begin":180,"end":513},"obj":"Sentence"},{"id":"T378","span":{"begin":514,"end":862},"obj":"Sentence"},{"id":"T379","span":{"begin":863,"end":1018},"obj":"Sentence"},{"id":"T380","span":{"begin":1019,"end":1241},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"The rationale of using chloroquine for treating COVID-19 patients is based on two potential and non–mutually exclusive mechanisms: antiviral activity and immunomodulatory effects. With regard to antiviral activity, chloroquine has been shown to inhibit various viruses in cell cultures, including SARS-CoV-1 and SARS-CoV-2, possibly via pH-dependent inhibition of virus–endosome fusion and/or posttranslational modifications of CoV proteins, although other mechanisms may also contribute [[32], [33], [34], [35]]. With regard to the immunomodulatory effects, the attenuated production of tumor necrosis factor alpha, interleukin (IL)-6 and interferons that follows the administration of chloroquine might help counteract an exaggerated proinflammatory response, which is thought to contribute to the organ damage observed in SARS-CoV-2–infected patients [36,37]. However, some authors have pointed out that an unfavourable immunomodulatory effect cannot be excluded, based on a reduced T helper 2 differentiation [38]. In our opinion, hydroxychloroquine should be preferred over chloroquine because of its less toxic profile (reduced ocular toxicity and fewer drug interactions) and its more potent in vitro activity against SARS-CoV-2 [39]."}

{"project":"2_test","denotations":[{"id":"32360444-15351731-22369771","span":{"begin":490,"end":492},"obj":"15351731"},{"id":"32360444-32203437-22369772","span":{"begin":508,"end":510},"obj":"32203437"},{"id":"32360444-9002011-22369773","span":{"begin":855,"end":857},"obj":"9002011"},{"id":"32360444-32194152-22369774","span":{"begin":1237,"end":1239},"obj":"32194152"}],"text":"The rationale of using chloroquine for treating COVID-19 patients is based on two potential and non–mutually exclusive mechanisms: antiviral activity and immunomodulatory effects. With regard to antiviral activity, chloroquine has been shown to inhibit various viruses in cell cultures, including SARS-CoV-1 and SARS-CoV-2, possibly via pH-dependent inhibition of virus–endosome fusion and/or posttranslational modifications of CoV proteins, although other mechanisms may also contribute [[32], [33], [34], [35]]. With regard to the immunomodulatory effects, the attenuated production of tumor necrosis factor alpha, interleukin (IL)-6 and interferons that follows the administration of chloroquine might help counteract an exaggerated proinflammatory response, which is thought to contribute to the organ damage observed in SARS-CoV-2–infected patients [36,37]. However, some authors have pointed out that an unfavourable immunomodulatory effect cannot be excluded, based on a reduced T helper 2 differentiation [38]. In our opinion, hydroxychloroquine should be preferred over chloroquine because of its less toxic profile (reduced ocular toxicity and fewer drug interactions) and its more potent in vitro activity against SARS-CoV-2 [39]."}